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Wu et al. |
2021 |
NOD/ltj T1D mice vs. ICR mice |
Decreased microbiota diversity and community richness were shown in animals before the onset of T1D.
T1D was associated with increased Firmicutes, Proteobacteria, and Deferribacteres phyla abundance.
Coprococcus 2, Lachnoclostridium_5, and Lachnospariceae_FCS020 genera (Firmicutes Phylum) were dominant in T1D, and their levels positively correlated with blood neutrophil ratios.
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[75] |
Ma et al. |
2020 |
Streptozotocin-induced T1D rats vs. control |
Firmicutes and Bacteroidetes are the dominant phyla in T1D rats.
Pathogenic bacteria are abundant in T1D rats, while beneficial bacteria are reduced compared to control.
Butyricicoccus and Allobaculum produce SCFAs and protect intestinal barrier function.
Imbalance of gut microbiota causes reduction of SCFAs and intestinal inflammation.
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[76] |
Prasad et al. |
2019 |
Angiotensin-converting enzyme 2 (ACE2) deficient T1D Akita mice vs. control |
Increased Firmicutes and Bacteroidetes in the gut of ACE2−/−Akita mice
ACE2 loss induced gut barrier permeability.
Dysbiosis in the gut promoted the development of diabetic nephropathy.
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[77] |
Patterson et al. |
2015 |
Streptozotocin (STZ) induced T1D in Sprague–Dawley rats (over time) vs. control |
Animals with T1D have decreased microbial diversity and differential expression of microbiota.
T1D onset was associated with an increase in Bacteriodetes: Firmicutes ratio.
Increased lactic acid-producing bacteria (Bifidobacterium and Lactobacillus) was associated with late-stage T1D progression.
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[78] |
Hara et al. |
2012 |
Virus-induced T1D rats vs. control |
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[79] |
Roesch et al. |
2009 |
Bio-breeding diabetes-prone (BB-DP) vs. bio-breeding diabetes-resistant (BB-DR) rats |
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[80] |
Brugman et al. |
2006 |
Diabetic BB-DP rats before and after the onset of diabetes in the presence and absence of antibiotics |
|